Interleukin (IL)-39 [IL-23p19/Epstein–Barr virus-induced 3 (Ebi3)] induces differentiation/expansion of neutrophils in lupus-prone mice. (12th August 2016)

• Record Type: Journal Article
• Authors: Wang, X; Liu, X; Zhang, Y; Wang, Z; Zhu, G; Han, G; Chen, G; Hou, C; Wang, T; Ma, N; Shen, B; Li, Y; Xiao, H; Wang, R
• Is Part Of: Clinical and experimental immunology. Volume 186:Number 2(2016:Nov.)
• Page Start: 144
• Page End: 156
• Publication Date: 2016-08-12
• Subjects: autoimmune diseases -- BAFF -- IL-39 -- lupus -- neutrophils; Immunopathology -- Periodicals; 616.079
• DOI: 10.1111/cei.12840
• Languages: English
• ISSNs: 0009-9104

Abstract

Summary: Interleukin (IL)-12 family cytokines play critical roles in autoimmune diseases. Our previous study has shown that IL-23p19 and Epstein–Barr virus-induced 3 (Ebi3) form a new IL-12 family heterodimer, IL-23p19/Ebi3, termed IL-39, and knock-down of p19 or Ebi3 reduced diseases by transferred GL7 + B cells in lupus-prone mice. In the present study, we explore further the possible effect of IL-39 on murine lupus. We found that IL-39 in vitro and in vivo induces differentiation and/or expansion of neutrophils. GL7 + B cells up-regulated neutrophils by secreting IL-39, whereas IL-39-deficient GL7 + B cells lost the capacity to up-regulate neutrophils in lupus-prone mice and homozygous CD19 cre (CD19-deficient) mice. Finally, we found that IL-39-induced neutrophils had a positive feedback on IL-39 expression in activated B cells by secreting B cell activation factor (BAFF). Taken together, our results suggest that IL-39 induces differentiation and/or expansion of neutrophils in lupus-prone mice. Graphical Abstract: